LncRNA FLVCR1-AS1 mediates miR-23a-5p/SLC7A11 axis to promote malignant behavior of cervical cancer cells

Zhou, Xi; Zhao, Xiujian; Wu, ZhouYi; Ma, Yan; Li, Heng

doi:10.1080/21655979.2022.2059958

Cited by 15 publications

(2 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Prior evidence has suggested that miR-23a-5p exhibits oncogenic activity in bladder cancer (Li et al 2018) and renal cell carcinoma (Quan et al 2017), and it can additionally influence tumorigenesis and disease progression through interactions with specific lncRNAs or mRNAs. In glioblastoma, for example, the lncRNATPT1-AS1 can promote growth activity through the sequestration of miR-23a-5p (Gao et al 2021), whereas the lncRNA FLVCR1-AS1 can enhance cervical cancer cell malignancy via the miR-23a-5p/SLC7A11 axis (Zhou et al 2022) and hepatoblastoma progression is at least partially driven by the SNHG9/miR-23a-5p/Wnt3a signaling pathway (Feng et al 2021). Besides affecting tumor progression, miR-23a-5p could modulate the innate host defense by promoting mycobacteria survival and inhibiting the activation of autophagy against Mycobacterium tuberculosis (M.tb.)…”

Section: Discussionmentioning

confidence: 99%

The linear ANRIL transcript P14AS regulates the NF-κB signaling to promote colon cancer progression

Ma,

2023

Mol Med

View full text Add to dashboard Cite

Background The linear long non-coding RNA P14AS has previously been reported to be dysregulated in colon cancer, but the mechanistic role that P14AS plays in colon cancer progression has yet to be clarified. Accordingly, this study was developed to explore the regulatory functions of ANRIL linear transcript-P14AS in cancer. Methods The expression of P14AS, ANRIL, miR-23a-5p and their target genes were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell supernatants of IL6 and IL8 were measured by Enzyme linked immunosorbent (ELISA) assay. Dual-luciferase reporter assays, RNA immunoprecipitation, or pull-down assays were used to confirm the target association between miR-23a-5p and P14AS or UBE2D3. Cell proliferation and chemosensitivity of NF-κB inhibitor BAY 11-7085 were evaluated by cell counting kit 8 (CCK8). Results When P14AS was overexpressed in colon cancer cell lines, enhanced TNF-NF-κB signaling pathway activity was observed together with increases in IL6 and IL8 expression. The Pita, miRanda, and RNA hybrid databases revealed the ability of miR-23a-5p to interact with P14AS, while UBE2D3 was further identified as a miR-23a-5p target gene. The results of dual-luciferase reporter, RNA pull-down, and RNA immunoprecipitation experiments confirmed these direct interactions among P14AS/miR-23a-5p/UBE2D3. The degradation of IκBa mediated by UBE2D3 may contribute to enhanced NF-κB signaling in these cells. Moreover, the beneficial impact of P14AS on colon cancer cell growth was eliminated when cells were treated with miR-23a-5p inhibitors or UBE2D3 was silenced. As such, these findings strongly supported a role for the UBE2D3/IκBa/NF-κB signaling axis as a mediator of the ability of P14AS to promote colon cancer progression. Conclusions These data suggested a mechanism through which the linear ANRIL transcript P14AS can promote inflammation and colon cancer progression through the sequestration of miR-23a-5p and the modulation of NF-κB signaling activity, thus highlighting P14AS as a promising target for therapeutic intervention efforts.

show abstract

Section: Discussionmentioning

confidence: 99%

The linear ANRIL transcript P14AS regulates the NF-κB signaling to promote colon cancer progression

Ma,

2023

Mol Med

View full text Add to dashboard Cite

show abstract

“…Multiple studies have suggested that FLVCR1-AS1 acts as an oncogene in multiple cancers through various ceRNA networks. Zhou et al got successful to reverse tumorigenesis of cervical cancer cells by suppressing FLVCR1-AS1 which resulted in increased miR-23a-5p expression level and decreased its target gene, SLC7A11, expression (Zhou, Zhao, et al 2022). Besides, Pan et al proved that miR-381-3p is sponged by FLVCR1-AS1 and CTNNB1.…”

Section: Discussionmentioning

confidence: 99%

LncRNA FLVCR1-AS1 functions as competing endogenous RNA (ceRNA) to sponge miR-381-3p and aggravate colorectal cancer via upregulation of Wnt signaling pathway

Beni,

Abdolvand,

Salehi

et al. 2023

Preprint

View full text Add to dashboard Cite

Introduction Colorectal cancer (CRC) is the third most frequent cancer and the second deadliest cancer, worldwide. Long non-coding RNAs (lncRNAs) have been introduced as vital regulators of CRC. lncRNA feline leukemia virus subgroup C receptor 1 antisense RNA 1 (FLVCR1‑AS1) is suggested to play a significant role in the tumorigenesis of several cancers. Wnt signaling pathway is the most deregulated pathway in CRC. The present study aimed to investigate the underlying mechanism of function of FLVCR1-AS1 in CRC through FLVCR1-AS1/miR-381-3p/ CTNNB1, LRP6, FZD3 axis. Methods The expression level of FLVCR1-AS1 was compared between CRC tissues and adjacent normal tissues, and additionally between CRC cell lines. Knockdown of FLVCR1-AS1 was performed in HCT116 cells, afterwards, the effects of this knockdown on the expression levels of FLVCR1-AS1, miR-381-3p, and three genes was examined via Real time-PCR. The differences in proliferation were evaluated using MTT assay, and cell death was assessed by flow cytometry. Results The results confirmed that FLVCR1-AS1 was upregulated in CRC tissues compared to adjacent normal tissues. RT-qPCR validated that FLVCR1-AS1 has the most level of expression in HT29, HCT116, SW480, and Caco2; respectively. Knockdown of FLVCR1‑AS1 was significantly followed by attenuated viability of HCT116 cells; while resulted in enhanced apoptosis and necrosis. Conclusion These findings support the idea that FLVCR1-AS1 may act as an oncogene in CRC and targeting FLVCR1-AS1/miR-381-3p/ CTNNB1, LRP6, FZD3 axis may be introduced as a novel target for CRC therapy and diagnosis in the future.

show abstract

Long non-coding RNAs as critical regulators and novel targets in cervical cancer: current status and future perspectives

et al. 2023

View full text Add to dashboard Cite

Cervical cancer is among the leading causes of cancer-associated mortality in women. In spite of vaccine availability, improved screening procedures, and chemoradiation therapy, cervical cancer remains the most commonly diagnosed cancer in 23 countries and the leading cause of cancer deaths in 36 countries. There is, therefore, a need to come up with novel diagnostic and therapeutic targets. Long non-coding RNAs (lncRNAs) play a remarkable role in genome regulation and contribute significantly to several developmental and disease pathways. The deregulation of lncRNAs is often observed in cancer patients, where they are shown to affect multiple cellular processes, including cell cycle, apoptosis, angiogenesis, and invasion. Many lncRNAs are found to be involved in the pathogenesis as well as progression of cervical cancer and have shown potency to track metastatic events. This review provides an overview of lncRNA mediated regulation of cervical carcinogenesis and highlights their potential as diagnostic and prognostic biomarkers as well as therapeutic targets for cervical cancer. In addition, it also discusses the challenges associated with the clinical implication of lncRNAs in cervical cancer.

show abstract

LncRNA FLVCR1-AS1 mediates miR-23a-5p/SLC7A11 axis to promote malignant behavior of cervical cancer cells

Cited by 15 publications

References 30 publications

The linear ANRIL transcript P14AS regulates the NF-κB signaling to promote colon cancer progression

The linear ANRIL transcript P14AS regulates the NF-κB signaling to promote colon cancer progression

LncRNA FLVCR1-AS1 functions as competing endogenous RNA (ceRNA) to sponge miR-381-3p and aggravate colorectal cancer via upregulation of Wnt signaling pathway

Long non-coding RNAs as critical regulators and novel targets in cervical cancer: current status and future perspectives

Contact Info

Product

Resources

About